Evidence mapPaperPMID 42166000Full record

ArticleMolecular and cellular biochemistry2026

Chronic bisphenol A exposure activates the cGAS-STING-NLRP3 axis driving persistent hippocampal neuroinflammation and cognitive impairment.

Veena V Tom, Sumit Mallick, Athira Sasidharan, Tanika Biswas, Bipasha Bose, Yogish Somayaji, Ronald Fernandes

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Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

7 authors.

Veena V TomDepartment of Allied Health Sciences, NGSM Institute of Pharmaceutical Sciences (NGSMIPS), Nitte (Deemed to Be University), Mangalore, Karnataka, 575018, India.
Sumit Mallick *Division of Molecular Genetics and Cancer, Nitte University Centre for Science Education and Research, Nitte (Deemed to be University), Karnataka, 575018, Mangalore, India.
Athira Sasidharan *Department of Allied Health Sciences, NGSM Institute of Pharmaceutical Sciences (NGSMIPS), Nitte (Deemed to Be University), Mangalore, Karnataka, 575018, India.
Tanika BiswasStem Cells and Regenerative Medicine Centre, Yenepoya Research Centre, Yenepoya (Deemed to Be University), University Road, Mangalore, Karnataka, 575018, India.
Bipasha BoseStem Cells and Regenerative Medicine Centre, Yenepoya Research Centre, Yenepoya (Deemed to Be University), University Road, Mangalore, Karnataka, 575018, India. bipasha.bose@yenepoya.edu.in.
Yogish SomayajiDepartment of Biochemistry and Biophysics, Texas A&M University, College Station, TX, USA. yogish_somayaji@tamu.edu.
Ronald FernandesDepartment of Pharmaceutical Chemistry, NGSM Institute of Pharmaceutical Sciences (NGSMIPS), Nitte (Deemed to Be University), Mangalore, Karnataka, 575018, India. ronaldfernandes@nitte.edu.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bisphenol A (BPA), a main component of polycarbonate plastics and epoxy resins, has been reported to cause chronic neuroinflammation and cognitive impairment in animal models. However, the precise molecular mechanisms of BPA-induced chronic neuroinflammation remain unknown. In this study, male C57BL/6 mice were administered BPA at different doses for one month, followed by a one-month washout period. We then conducted behavioral tests, oxidative stress assays, and immunohistochemistry to quantify neuronal density and the activation of microglia and astrocytes in the central nervous system. We also carried out RT-qPCR gene expression analysis of the hippocampus for the cGAS-STING-NLRP3 pathway, cytokine assays, and microglial markers to decipher the immune responses in the hippocampus following BPA exposure. BPA induced dose-dependent behavioral deficits, which were most pronounced at 50 mg/kg. These findings suggest that cGAS-STING signaling acts as a key upstream mediator of BPA-induced hippocampal neuroinflammation and cognitive dysfunction.

Indexed as

Benzhydryl CompoundsCognitive DysfunctionHippocampusMembrane ProteinsNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinNucleotidyltransferasesPhenolsSignal TransductionAnimalsBisphenol A CompoundscGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMaleMiceMice, Inbred C57BLBenzhydryl Compoundsbisphenol ABisphenol A CompoundscGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseNucleotidyltransferasesPhenolsSting1 protein, mouseSTING ProteinBisphenol A, Neuroinflammation, cGAS–STING pathway, NLRP3 inflammasome, C57BL/6 mice, Neurotoxicity

Identifiers

PMID42166000

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.